It has been demonstrated that the most important load compensation mechanisms are the force-length and force-velocity relationships of the diaphragm and two neural reflexes which increase respiratory drive. These are the vagally-dependent prolongation of inspiration which increases the peak activity of the phrenic nerve and external intercostal muscles, and the progressive increase in neural drive during continuous loading which is dependent on the progressive increase in peripheral chemoreceptor stimuli. Although a number of studies have examined the effects of anesthesia in man and in animals on the responses to mechanical loads, these studies have their limitations. They include the failure to examine the effects of clinically relevant inhalational anesthetics (halothane and enflurane), and to measure the decrease in functional residual capacity (FRC) as a result of anesthesia which is a major variable in load response (force-length relationship of the diaphragm). There are no neurophysiological studies on the effects of general anesthetics on the load adjustment mechanisms or on the responses to CO2 or hypoxemia. The proposed studies will examine and compare the effects of halothane and enflurane in cats and humans on mechanical load compensation. The studies on cats will measure the tidal volume, airway pressure and the neural reflex responses to single breath and to continuous inspiratory elastic loads and to tracheal occlusion applied at FRC, and also these responses to CO2 and to hypoxemia. The effects of bilateral cervical vagotomy as well as changes in FRC will also be examined. The data will also be compared to the investigator's pre-existent data on cats anesthetized with chloralose and urethane. The human studies will examine the load and CO2 responses while awake and during anesthesia with enflurane and with halothane. Both the FRC and configurational changes of the rib cage will be measured.